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Researchers were able to reverse memory loss in mice with Alzheimer's disease by interfering with an enzyme responsible for blocking memory formation. Although the enzyme’s function has been known for years, researchers had not been able to block its effects on cognition without causing far worse side effects - until now. The team hopes to repeat the results on humans.

Scientists at Massachusetts Institute of Technology reversed memory loss in mice by interfering with an enzyme known as HDAC2 that contributes to memory decline. This same enzyme is also present in humans, and is overproduced in Alzheimer’s patients, causing similar memory inhibition, MIT News reported. The researchers hope they can develop a drug that can interfere with HDAC2 function in humans, which may help to reverse some of the memory problems associated with Alzheimer’s disease.

What makes this finding so significant is that the scientists were able to interfere with the enzyme without causing other health concerns for the mice. Study senior author Li-Huei Tsai first identified HDAC2's role in learning and memory in 2007. However, until now, she and her team were unable to successfully interfere with HDAC2's behavior without also creating other unpleasant and even deadly side effects.

How It Works

HDAC2 works by turning off the genes that allow mice (and humans) to form new memories. It does this by condensing the genes tightly together so that they can’t be expressed, and in turn can’t do their job. The problem is, genes and the enzymes that interact with them often serve double purposes. Interfering with one enzyme for a specific outcome could result in several unforeseen and unwanted results.

Previous efforts to interfere with HDAC2 have also interfered with another very closely related enzyme called HDAC-1. This related enzyme plays a vital role in the production of white and red blood cells, as well as the creation of other types of cells. Interfering with its behavior has serious consequences, a statement on the study reported. Now, 10 years later, Tsai believes she has finally figured out a way to interfere with HDAC2 without also inhibiting HDAC-1.

To test this, the team identified a gene that works specifically to recruit HDAC2 to Alzheimer’s related genes, without interfering with HDAC-1. While they deactivated the Sp3 gene in mice with Alzheimer’s disease, HDAC2 was not called to interfere with memory genes, and so the mice with Alzheimer’s were able to form long-term memories again.

Turning off genes in special genetically modified mice may be easy enough, but it's not feasible for humans. Researchers needed to figure out a more realistic way to get rid of Sp3 in the body. They accomplished this by engineering neurons that help to collect all the Sp3 in the brain, and prevent it from binding to HDAC2. This resulted in the same reversal of memory loss, and also did not have the adverse side effects on blood cell production.

The research is still in its early stages and it will likely take time before models will be tested on people. Still, the researchers are hopeful their study could one day lead to more effective Alzheimer’s treatments.

"We think that HDAC2 serves as a master regulator of memory gene expression," said study author Tsai in a recent statement."If we can remove the blockade by inhibiting HDAC2 activity or reducing HDAC2 levels, then we can remove the blockade and restore expression of all these genes necessary for learning and memory."